The goal of this project is to learn more about the control of movement in normal humans and in patients with voluntary movement disorders such as Parkinson's disease, cerebellar ataxia, hemiplegia from stroke and dystonia. The tools we use include clinical neurophysiological methods such as electroencephalography, electromyography, and transcranial magnetic stimulation and neuroimaging with positron emission tomography and functional magnetic resonance imaging. Currently active projects in the Section include analysis of the bradykinesia in Parkinson?s disease, studies of recovery from hemiplegia, and the physiology of dystonia. One major scientific target of the Branch is to understand and possibly influence cortical reorganization in patients with congenital or acquired lesions of the central nervous system. A multi-modality approach (neuroimaging with PET and functional MRI, EEG, and transcranial magnetic stimulation) is being used to determine patterns of long-term reorganization of functional brain topography in individual stroke patients. The analysis reveals the best recovery of function comes from reorganization of the damaged hemisphere rather than the contralateral one. In order to explain why people more likely to fall backward than forward, we have been studing subjects perturbed by a translational pushing device. We found that limitations to balance can be predicted by position and velocity of the center of mass of the body. Asymmetry of the tendency to fall is due in part to the asymmetry of the functional foot length. We have done studies of the EEG activity associated with different movements in patients with dystonia. The results indicate that the expected change in movement related potentials with increased complexity does not occur. This may indicate a problem in the process of selection of movements to be made. We are using transcranial magnetic stimulation to investigate the processes of inhibition that occur in muscles that are not selected for particular movements. There appear to be multiple mechanisms. We intend to see if inhibition of any type is defective in patients with dystonia. We are also doing clinical neurophysiological studies of patients with dystonia and their asymptomatic relatives, looking to see if we can find a marker of a genetic propensity to develop dystonia. We have conducted a study to see if training to improve sensory acuity would improve patients with focal limb dystonia. Results do demonstrate improvement in both sensory acuity and motor performance, but the improvement in motor performance is limited in magnitude.